Three cheers for Marie for the longest post ever!!

Now you're talking!if he wants to be famous

But seriously that's what we want: a lot of people who want to publish would be good for all of us.
The more the better.
In addition to being a brilliant researcher and clinician, Dr. Calabresi is a hell of a nice guy. It would be nice, though, if he could figure out just what the hell is wrong with me...Most of us do NOT think venous pathology causes the MS, but rather may be a result of the plaques and scar tissue. The authors also say the same at the end of that article.
But how can inflammation and damage deep inside the brain cause stenoses "miles" away, outside the skull and the spine? If that is correct, inflammation at the thighs could very well lead to stenoses of the coronary arteries an lead to instant death.Most of us do NOT think venous pathology causes the MS, but rather may be a result of the plaques and scar tissue. The authors also say the same at the end of that article.
marcstck wrote:I forwarded the Italian paper on to Dr. Peter Calabresi at Johns Hopkins, one of the top two or three MS guys in the United States. Here is the rather short response he sent me today:
In addition to being a brilliant researcher and clinician, Dr. Calabresi is a hell of a nice guy. It would be nice, though, if he could figure out just what the hell is wrong with me...Most of us do NOT think venous pathology causes the MS, but rather may be a result of the plaques and scar tissue. The authors also say the same at the end of that article.
Dr. Calebresi may be a nice guy, but he didn't read the conclusion thoroughly. Here is the conclusion. Let's read it for ourselves. Zamboni does not agree with your doctor, Marc. On the contrary, he make the point that if the demyelinating lesions were creating the venous obstructions, those patients on immune modulating medicine would NOT have as many stenoses. (Their inflammation and lesions would, having been dampened, create less venous obstruction.) BUT, the opposite is true. Venous obstruction was found in only MS patients, no matter how they were being treated.Moreover, the absence of Doppler and venographic features of CCSVI in controls suggests that venous obstructions may be causative of MS rather than a coincidental finding.
Interestingly, similar venous stenoses considered to be congenital
malformations have been described in other human diseases, i.e.,
membranous obstruction of the inferior vena cava and a minor group of
chronic venous diseases of the lower limbs.27-28 Such venous obstruction
brings about an insufficient venous drainage, respectively at the level of the liver and of the cutaneous tissue, subsequently causing inflammation,
sclerosis, and degenerative lesions.24-25,36 In contrast with the malformation hypothesis, cases have been reported of white cell infiltration and endophlebohypertrophy in venous valves where
endocarditis is present.37
Even though this correlation has never been studied in MS, reports of
valvulitis in the course of significant inflammatory disease should certainly be taken into consideration since they support the hypothesis that these
malformations are a result of CDMS rather than a cause. However, if vessel abnormalities were due to an inflammatory-autoimmune disease, they would be less frequent in patients treated with immunomodulating/immunosuppressant agents. On the contrary, our analysis in the RR-SP group did not demonstrate an increased number of extracranial venous stenosing lesions in untreated as compared to treated patients.